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Discussion In this study we evaluated the effects of discontinuing pamidronate treatment in children and adolescents with OI who had received at least three years of treatment. We found evidence that bone turnover increased, whereas areal BMD z-scores decreased during the two years following treatment discontinuation. Stopping treatment had no detectable effect on fracture incidence and functional status. These findings are similar to observations that have been made in adults who discontinued bisphosphonate treatment mostly with oral alendronate ; after prolonged therapy 18, 19 ; . Even though the activity of bone resorption increased after treatment discontinuation, urinary NTX excretion still remained well below pretreatment levels, which is also similar to findings in adults 18, 19 ; . This suggests that the pamidronate that is buried in the bone tissue during intravenous treatment cycles does have biological activity for at least two years after the last dose of the drug is given. Although areal BMD z-scores at the lumbar spine decreased after treatment discontinuation, these changes were small and slow compared to the increases that are seen when pamidronate is started in children and adolescents with OI 4 ; . Consequently, areal BMD z-scores remained well above pretreatment levels. It should be noted that a decrease in areal BMD z-scores does not mean that these patients experienced bone loss. Quite to the contrary, they continued to gain bone mass i.e. bone mineral content ; even after pamidronate treatment was stopped. However the gain in bone mass was less than what would be expected in healthy subjects who experience a similar increase in bone size i.e. area ; . Consequently, areal BMD did not rise as fast as in healthy subjects, leading to a decline in z-scores. 11.
Patients were randomized to receive zoledronic acid, pamidronate , or placebo every 3-4 weeks for up to 24 months prostate cancer, breast cancer, and.
Pamidronate reduces the number of skeletal complications in women with metastatic breast cancer.
0.19 mol L for the bovine kidney enzyme with pyridoxal 5 -phosphate is compatible with the observed bovine plasma pyridoxal phosphate concentration of 0.3 mol L 19 ; . Several lines of evidence suggest that alkaline phosphatase is the enzyme primarily responsible for pyridoxine phosphate phosphatase activity in serum. The lack of alkaline phosphatase activity in hypophosphatasia is associated with markedly increased pyridoxal 5 -phosphate concentrations in plasma 20 ; . Inactivating the tissue nonspecific alkaline phosphatase gene in mice also leads to similar abnormalities of vitamin B-6 metabolism 21 ; . Lumeng and Li 22 ; concluded that pyridoxal phosphate hydrolase activity in rat liver was identical with alkaline phosphatase. The subcellular fraction with the most activity was the nuclear fraction, which contained the plasma membrane fragments. This is consistent with the evidence that tissue nonspecific alkaline phosphatase is an ectoenzyme. In the current study, pyridoxine phosphate phosphatase activity at pH 7.4 in diluted serum was highly correlated r 0.95; P 0.001 ; with the clinical assay for alkaline phosphatase using p-nitrophenyl phosphate at pH 10.3. Therefore, we conclude that the pyridoxine phosphate phosphatase activity in serum is due to alkaline phosphatase. Other workers have commented on substrate inhibition of pyridoxine phosphatase 23, 24 ; . We found it to have a detectable effect at concentrations as low as 10 mol L. The possibility that phosphate exerts a mixed inhibition effect has also been mentioned previously. Fernley and Walker 25 ; noted that although phosphate inhibition was predominantly competitive, there was a mixed component in calf intestinal alkaline phosphatase. However, for the conditions used in our study, omitting the uncompetitive inhibition term had little effect on the results. Fernley and Walker also noted that although 1 mmol L magnesium ion stimulated the hydrolysis of 4-methylumbelliferyl phosphate, it caused over 50% inhibition of the hydrolysis of pyrophosphate and ATP. As the magnesium ion concentration in serum is approximately 1 mmol L, phosphomonoesterase activity is probably predominant. They reported that the Ki for inor.
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The PTH. This is not surprising given the nature of the disease. Parathyroid carcinoma is the most severe and aggressive form of primary hyperparathyroidism and often loses responsiveness to interventions to which less severe forms of primary hyperparathyroidism respond 1 ; . The escape of responsiveness to the calcimimetic could be explained by a number of scenarios, including further dedifferentiation of the cancer, increased growth of the tumor, or tumor metastases. Perhaps the most surprising aspect of the patient's response is the maintenance of a relatively stable serum calcium level in the face of an increasing serum PTH level. As the drug is apparently becoming less effective at the level of the parathyroid cell, one would have to evoke either renal or bone effects of the drug to explain this. The observations that.
20 half were given a placebo infusion for two years and half received monthly pamidronate boluses and papaverine.
Fifty-two heavily pre-treated patients with painful radiographically confirmed and progressing bone metastases were randomised to receive either a two-hour infusion of pamidronate 120 mg in 1000 ml 0.9% saline infusion group I ; or an identical infusion of saline alone group II ; . Randomisation was performed without stratification using an envelope system retained in the pharmacy. Four weeks later, or earlier in the event of worsening symptoms n 13 ; , all patients received an infusion of pamidronate 120 mg. Thereafter patients experiencing subjective benefit received further infusions when their symptoms worsened again. The pretreatment characteristics of the study population are shown in Table 1. All patients had received at least one previous systemic anticancer treatment. No concomitant systemic anticancer treatment or radiotherapy during the course of the study was allowed, with the exception of endocrine therapy which was continued to avoid the possibility of a tumour response to withdrawal of hormone treatment. Bisphosphonates and other drugs known to affect bone metabolism in the previous three months were not allowed. Analgesics were prescribed as necessary. The study was approved by the South Sheffield Research Ethics Committee and all patients gave their written informed consent to participate. Patients were followed in the out-patient department every two weeks for 12 weeks and then monthly thereafter. Four patients were not evaluable for clinical response three in the pamidronate group and one in the placebo group ; . Three of them died soon after entering the trial and one did not have clinical data available. As a result 48 patients 22 group I and 26 group II ; were evaluable for clinical response. A further two patients did not provide urine samples one in each group ; and were not evaluable for biochemical response. To establish a control group for bone turnover markers, we enrolled 40 healthy volunteers who also were not taking any drugs known Table 1. Baseline characteristics of clinically evaluable patients.
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112 ADEQUATE DIALYSIS DESPITE REVERSED USE OF TEMPORARY CATHETERS. C. Dipchand, K. Jindal, T. Keough-Ryan, K. Thompson, D. Hirsch, Medicine, Dalhousie University, Halifax. Central venous catheters CVC ; are being used more frequently as dialysis access in an aging population. The reported rate in the literature of CVC recirculation RC ; is usually 10% for catheters in the straight position. Few studies have looked at the RC in malfunctioning CVCs run in the reversed direction. The relationship between RC and adequacy of dialysis is still under investigation. This was a prospective observational cohort study assessing CVC recirculation in the prevalent chronic hemodialysis HD ; population in an academic centre. The RC at a blood flow of 200ml min was measured monthly a mean of 2 readings ; by ultrasound dilution technique AmJ Kidney Dis.1998: 32 6 ; : 1046 ; for 3 months. Demographic and other data including location of CVC, length of CVC, straight or reverse position of CVC, use of warfarin for maintenance of access, use of tPa for catheter dysfunction and changing of catheter reason for the change were collected prospectively. Monthly urea reduction ratio URR ; was used to measure dialysis adequacy. 76 patients were eligible and included in the study. 55% female, 49% diabetic, 96% temporary CVC. 72% of the CVCs each month were run in the reversed position because of catheter malfunction. The mean 95%CI ; RC was 7.44% 5.75-9.12 ; , 7.03% 5.27-8.79 ; and 6.73% 4.96-8.49 ; for months 1, 2 and 3 respectively. Mean 95%CI ; URR was 68.9% 66.9-70.8 ; , 67.8% 66.1-69.5 ; and 69.2% 67.5-70.9 ; for the same time periods. The Pearson correlation coefficient for the relationship between URR and RC was -0.21, p 0.067. The rates of recirculaton reported here are consistent with those already reported in the literature despite the fact that the majority of the catheters in this study were run in the reversed direction. There is little correlation between URR and RC in this dialysis population with temporary CVCs. 113 SHOULD HIGH RISK HLA HAPLOTYPES EXCLUDE ABORIGINAL SUBJECTS FROM KIDNEY DONATION? Roland F. Dyck, Division of Nephrology, University of Saskatchewan, Saskatoon. Canadian Aboriginal people are experiencing an epidemic of type 2 diabetes and diabetic end-stage renal disease. Living donor renal transplantation is being promoted within this population; however, such donors may be at high risk of developing diabetes and diabetic complications themselves. We have recently reported an increased frequency of specific HLA haplotypes in younger vs. older Aboriginal subjects with diabetic end-stage renal disease 1 ; . Over 65% of young 50 years ; Aboriginal subjects with diabetic end-stage renal disease had either an A2 DR4 or A2 DR8 haplotype odds ratio 5.09; confidence intervals 1.35, 20.15 ; vs. older Aboriginal subjects with diabetic end-stage renal disease. Forty % of young Aboriginal subjects with diabetic end-stage renal disease were homozygous for at least one of A2, DR4 or DR8. Of particular concern is that these HLA antigens have been shown to occur at high frequencies in other populations with both type 1 and type 2 diabetes. Since most potential living donors are related to the potential recipients of their kidney, there may be particular risks for Aboriginal donors in performing this widely accepted form of altruism. Therefore, transplant programs that deal with Aboriginal patients with diabetic end-stage renal disease have an additional responsibility to consider the risks for their potential donors. The following recommendations are presented with respect to potential Aboriginal kidney donors: First, further studies should be carried out in other centers to substantiate refute our findings. Consideration should be given to excluding potential Aboriginal donors on the basis of their HLA haplotypes if these findings are confirmed. Second, potential donors with high risk HLA haplotypes should be informed that they may have a genetic propensity to develop diabetes and its complications. Third, this risk should be considered in the context of other environmental risk factors such as maternal history of diabetic pregnancy, obesity, and degree of physical activity. Fourth, a glucose tolerance test and measures of insulin resistance should be carried out in such subjects. Fifth, such potential living donors should receive detailed education with respect to lifestyle changes that may reduce their risks. 1. R.Dyck, C. Bohm, H. Klomp: Increased Frequency of HLA A2 DR4 and A2 DR8 Haplotypes in Young Saskatchewan Aboriginal People with Diabetic End-Stage Renal Disease. J Nephrol 2003; 23: 178-185 and parnate.
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Abbreviations: bcva, best-corrected snellen visual acuity; cme, cystoid macular edema; imt, immunomodulatory therapy; ivig, intravenous immunoglobulin; logmar, logarithm of the minimum angle of resolution; na, not applicable; nsaids, nonsteroidal anti-inflammatory drugs; oct, optical coherence tomography; od, right eye; os, left eye; va, visual acuity.
To the Editor After lengthy discussion of the definition, pathogenesis, natural history, and prognosis of lacunes, Millikan and Futrell1 conclude that "a lacune is a stroke, just a small one." The need for a better definition of the old label "lacune" had already been envisaged.2"4 The label lacune is attributed to the pathological lesion as such4 and should not be applied to the computed tomography CT ; magnetic resonance imaging picture or to the clinical syndrome. Indeed, if the brain is examined at the onset of the clinical picture or shortly thereafter, the low-density area revealed by the CT scan surely cannot be related to a lacune, but to an ischemic infarction of restricted size, which usually evolves into a cavity, or more rarely, glial mesodermal scar tissue.5 I agree completely with those who hold that lacune is one of the many misleading diagnostic labels used in clinical neurology. Moreover, I would add some brief additional comments to Millikan and Futrell's review. I do not believe that "the neuropathologist's and the radiologist's definitions of a lacune are clear."1 Radiologists should give a description of the image, in terms of density level, size, shape, and location of the involved area. The term lacune is only a pathological one. As to the pathogenesis of lacune, 1 in our experience3 patients with lacunar lesions and related clinical syndromes were more often hypertensive than both nonvascular controls 75.3% versus 35.1%, p 0.0005 ; and ischemic controls as well 75.3% versus 59.5%, ; 0.001 ; . In normotensive patients about 30% of cases ; , embolism from the large arteries or from the heart could have been responsible.6 Intracerebral small-vessel occlusion was often underestimated as a cause of ischemic lesions because, in the pathophysiology of cerebral ischemia, emphasis has been placed on the involvement of large cranial arteries rather than on the obstruction of small ones. However, intracerebral small-vessel occlusion, regardless of its origin, should be held responsible for microinfarctions, especially deep ones.7 In our experience, 8 the survival rate of lacunar patients was 479 1, 000, definitively lower than the survival rate of the normal population 755 1, 000 ; . The survival rate curve in patients with CT lacunar images was slightly higher than that of completed stroke due to large infarcts, but considerably lower than that of patients with reversible ischemic attacks. Life expectancy was significantly shortened if the patient was hypertensive, 65 years of age, or exhibited a poor functional recovery and paromomycin.
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Drug regimens are listed as total dose per day, either single dose or divided dose, whichever is customary. LDL indicates low-density lipoprotein. Calculated as a weighted mean.
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For future clean-up, the EPA will continue to oversee the project to ensure that the actions are acceptable and adequately protective of the environment. Officials from both the Justice Department as well as the U.S. Attorney's Office for the Northern District of Iowa believe the settlement was a major success. Specifically, Ronald J. Tenpas, Acting Assistant Attorney General, stated that "CERCLA's goals will be vindicated through the proposed settlement because the responsible parties agreed to cooperate, reimburse the United States' costs, and perform response actions at the Site.
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A 50-yr-old Caucasian woman was diagnosed with multiple myeloma in 1996 and received three cycles of vincristine, doxorubicin, and dexamethasone, followed by tandem stem cell transplantation. The patient was treated with a short course of interferon- in early 1997 but never received total-body irradiation or thalidomide. In July 1996, she was started on pamidronate at 90 mg IV monthly; this dose was increased to 180 mg IV monthly in January 1998. In October 1999, the patient had a serum creatinine of 0.5 mg dl, and pamidronate therapy was increased to 180 mg IV bimonthly. Subsequently, the creatinine increased to 2.3 mg dl in December 1999 and to 2.8 mg dl in January 2000. At that time, the patient developed full nephrotic syndrome, with 24-h urinary protein excretion of 5.8 g d, albumin of 2.8 g dl, and peripheral edema. A renal biopsy was performed in January 2000. After 3 mo of follow-up monitoring, the patient continued to receive pamidronate, had a serum creatinine of 7.5 mg dl, and began hemodialysis and pediatric.
Pediatric studies on this medicine have been done only in adult patients, and there is no specific information comparing use of pamidronate in children with use in other age groups.
1. Adami, S., Bhalla, A. K., Dorizzi, R., Montesanti, F., Rosini, S., Salvagno, G., et al. The acute-phase response after bisphosphonate administration. Calcif Tissue Int 41: 326 331; Adami, S., Mian, M., Gatti, P., Rossini, M., Zamberlan, N., Bertoldo, F., et al. Effects of two oral doses of alendronate in the treatment of Paget's disease of bone. Bone 15: 415417; 1994. Adami, S., Salvagno, G., Guarrera, G., Montesanti, F., Garavelli, S., Rosini, S., et al. Treatment of Paget's disease of bone with intravenous 4-amino-1hydroxybutylidene-1, 1-bisphosphonate. Calcif Tissue Int 39: 226 229; Adami, S., Zamberlan, N., Mian, M., Dorizzi, R., Rossini, M., Braga, B., et al. Duration of the effects of intravenous alendronate in postmenopausal women and in patients with primary hyperparathyroidism and Paget's disease of bone. Bone Miner 25: 7582; 1994. Adami, S., Zamberlan, N., Mian, M., Dorizzi, R., Rossini, M., Braga, B., et al. Duration of the effects of intravenous alendronate in postmenopausal women and in patients with primary hyperparathyroidism and Paget's disease of bone. Bone Miner 25: 7582; 1994. Adamson, B. B., Gallacher, S. J., Byars, J., Ralston, S. H., Boyle, I. T., and Boyce, B. F. Mineralisation defects with pamidronate therapy for Paget's disease. Lancet 342: 1459 1460 and pegasys.
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| Disodium pamidronate chemistry1. Rodan GA, Fleisch HA. Bisphosphonates: mechanisms of action. J Clin Invest 1996; 97: 26922696 Markowitz GS, Appel GB, Fine PL et al. Collapsing focal segmental glomerulosclerosis following treatment with high-dose pamidronate. J Soc Nephrol 2001; 12: 11641172 Markowitz GS, Fine PL, Stack JI et al. Toxic acute tubular necrosis following treatment with zoledronate Zometa ; . Kidney Int 2003; 64: 281289 Julian B, Laskow D, Dubovsky J, Dubovsky EV, Curtis J, Quarles LD. Rapid loss of vertebral bone mineral density after renal transplantation. N Engl J Med 1991; 325: 544550 Cueto-Manzano AM, Konel S, Hutchison AJ et al. Bone loss in long term renal transplantation: histopathology and densitometry analysis. Kidney Int 1999; 55: 20212029 Durieux S, Mercadal L, Orcel P et al. Bone mineral density and fracture prevalence in long-term kidney graft recipients. Transplantation 2002; 74: 496500 Fan SLS, Almond MK, Ball E, Evans K, Cunningham J. Pamidronate therapy as prevention of bone loss following renal transplantation. Kidney Int 2000; 57: 684690 Coco M, Glicklich D, Faugere MC et al. Prevention of bone loss in renal transplant recipients: a prospective, randomized trial of intravenous pamidronate. J Soc Nephrol 2003; 14: 26692676 and pamidronate.
Therapy on cortical and trabecular bone: comparison with estrogen. J Med. 90: 171-178. Khokher MA, Dandona P. 1989 Diphosphonates inhibit human osteoblast secretion and proliferation. Metabolism. 38: 184-187. Boonekamp PM, van der Wee-Pals LJA, Van Wijk-van Lennep MML, Thesing CW, Bijvoet OLM. 1986 Two modes of action of bisphosphonates on osteoclastic resorption of mineralized matrix. Bone Mineral. 1: 27-39. Sato M, Grasser W, Endo N, et al. 1991 Bisphosphonate action. Alendronate localization in rat bone and effects on osteoclast ultrastructure. J Clin Invest, 88: 2095-2105. Hughes DE, MacDonald BR, Russell RGG, Gowen M. 1989 Inhibition of osteoclast-like cell formation by bisphosphonates in longterm cultures of human bone marrow. J Clin Invest. 83: 1930-1935. Carano A, Teitelbaum SL, Konsek JD, Schlesinger PH, Blair HC. 1990 Bisphosphonates directly inhibit the bone resorption activity of isolated avian osteoclasts in vitro. J Clin Invest. 85: 456-461. Lin JH, Duggan DE, Chen I-W, Ellsworth RL. 1991 Physiological disposition of alendronate, a potent anti-osteolytic bisphosphonate, in laboratory animals. Drug Metab Dispos. 19: 926-932. Reginster JY, Deroisy R, Denis D, et al. 1989 Prevention of postmenopausal bone loss by tiludronate. Lancet. 2: 1469-1471. Devogelaer JP, Nagant de Deuxchaisnes C. 1990 Treatment of involutional osteoporosis with the bisphosphonate APD disodium pamidronate ; : non-linear increase of lumbar bone mineral density [Abstract]. J Bone Mineral Res. 5 Suppl 2 ; : S251. Passeri M, Baroni MC, Pedrazzoni M, et al. 1991 Intermittent treatment with intravenous 4-amino-l-hydroxybutylidene-l, l-bisphosphonate AHBuBP ; in the therapy of postmenopausal osteo and pegfilgrastim.
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